Abstract
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder. AD is characterized by the production and aggregation of beta-amyloid (Aβ) peptides, hyperphosphorylated tau proteins that form neurofibrillary tangles (NFTs), and subsequent neuroinflammation, synaptic dysfunction, autophagy and oxidative stress. Non-coding RNAs (ncRNAs) can be used as potential therapeutic targets and biomarkers due to their vital regulatory roles in multiple biological processes involved in disease development. The involvement of ncRNAs in the pathogenesis of AD has been increasingly recognized. Here, we review the ncRNAs implicated in AD and elaborate on their main regulatory pathways, which might have contributions for discovering novel therapeutic targets and drugs for AD.
Highlights
Reviewed by: Karen Schmitt, Central Institute of Mental Health (ZI), Germany Douglas Gordon Walker, Shiga University of Medical Science, Japan
The findings reported by Li et al revealed markedly increased levels of miR-613 in the serum and cerebral spinal fluid (CSF) of patients with mild cognitive impairment (MCI) and dementia of the Alzheimer’s type (DAT), as well as in the hippocampus of amyloid precursor protein (APP)/PS1 transgenic mice (Li et al, 2016)
The levels of miR-29a/b-1 and miR-29c were decreased in the brains of patients with sporadic Alzheimer’s disease (AD) in other studies, and levels of both the β-site APP cleaving enzyme 1 (BACE1) mRNA and protein were increased by targeting BACE1 expression through these miRNAs (Hebert et al, 2008; Lei et al, 2015)
Summary
MiR188-3p is capable of functionally binding to the 3 -UTR of the BACE1 mRNA, and the overexpression of miR-188-3 in the hippocampus of 5XFAD TG mice suppresses BACE1 expression to reduce Aβ production and prevent synaptic dysfunction (Zhang J. et al, 2014). The levels of miR-29a/b-1 and miR-29c were decreased in the brains of patients with sporadic AD in other studies, and levels of both the BACE1 mRNA and protein were increased by targeting BACE1 expression through these miRNAs (Hebert et al, 2008; Lei et al, 2015).
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